For a broader coverage related to this topic, see Kinesiology.

Exercise physiology is the study of the acute responses and chronic adaptations to a wide range of physical exercise conditions. In addition, many exercise physiologists study the effect of exercise on pathology, and the mechanisms by which exercise can reduce or reverse disease progression. Accreditation programs exist with professional bodies in most developed countries, ensuring the quality and consistency of education. In Canada, one may obtain the professional certification title - Certified Exercise Physiologist for those working with clients (both clinical and non clinical) in the health and fitness industry.

An exercise physiologist's area of study may include but is not limited to biochemistry, bioenergetics, cardiopulmonary function, hematology, biomechanics, skeletal muscle physiology, neuroendocrine function, and central and peripheral nervous system function. Furthermore, exercise physiologists range from basic scientists, to clinical researchers, to clinicians, to sports trainers.

Humans have a high capacity to expend energy for many hours during sustained exertion. For example, one individual cycling at a speed of 26.4km/h (16.4mph) over 8,204km (5,098mi) during 50 consecutive days may expended a total of 1,145 MJ (273,850 kcal; 273,850 dieter calories) with an average power output of 182.5 W.[1]

Skeletal muscle burns 90mg (0.5 mmol) of glucose each minute during continuous activity (such as when repetitively extending the human knee),[2] generating 24 W of mechanical energy, and since muscle energy conversion is only 22-26% efficient,[3] 76 W of heat energy. Resting skeletal muscle has a basal metabolic rate (resting energy consumption) of 0.63 W/kg[4] making a 160 fold difference between the energy consumption of inactive and active muscles. For short duration muscular exertion, energy expenditure can be far greater: an adult human male when jumping up from a squat mechanically generates 314 W/kg, and such rapid movement can generate twice this in nonhuman animals such as bonobos,[5] and in some small lizards.[6]

This energy expenditure is very large compared to the resting metabolism basal metabolic rate of the adult human body. This varies somewhat with size, gender and age but is typically between 45 W and 85 W.[7][8] Total energy expenditure (TEE) due to muscular expended energy is much higher and depends upon the average level of physical work and exercise done during a day.[9] Thus exercise, particularly if sustained for very long periods, dominates the energy metabolism of the body.

Energy needed to perform short lasting, high intensity bursts of activity is derived from anaerobic metabolism within the cytosol of muscle cells, as opposed to aerobic respiration which utilizes oxygen, is sustainable, and occurs in the mitochondria. The quick energy sources consist of the phosphocreatine (PCr) system, fast glycolysis, and adenylate kinase. All of these systems re-synthesize adenosine triphosphate (ATP), which is the universal energy source in all cells. The most rapid source, but the most readily depleted of the above sources is the PCr system which utilizes the enzyme creatine kinase. This enzyme catalyzes a reaction that combines phosphocreatine and adenosine diphosphate (ADP) into ATP and creatine. This resource is short lasting because oxygen is required for the resynthesis of phosphocreatine via mitochondrial creatine kinase. Therefore, under anaerobic conditions, this substrate is finite and only lasts between approximately 10 to 30 seconds of high intensity work. Fast glycolysis, however, can function for approximately 2 minutes prior to fatigue, and predominately uses intracellular glycogen as a substrate. Glycogen is broken down rapidly via glycogen phosphorylase into individual glucose units during intense exercise. Glucose is then oxidized to pyruvate and under anaerobic condition is reduced to lactic acid. This reaction oxidizes NADH to NAD, thereby releasing a hydrogen ion, promoting acidosis. For this reason, fast glycolysis can not be sustained for long periods of time. Lastly, adenylate kinase catalyzes a reaction by which 2 ADP are combined to form ATP and adenosine monophosphate (AMP). This reaction takes place during low energy situations such as extreme exercise or conditions of hypoxia, but is not a significant source of energy. The creation of AMP resulting from this reaction stimulates AMP-activated protein kinase (AMP kinase) which is the energy sensor of the cell. After sensing low energy conditions, AMP kinase stimulates various other intracellular enzymes geared towards increasing energy supply and decreasing all anabolic, or energy requiring, cell functions.[citation needed]

Plasma glucose is said to be maintained when there is an equal rate of glucose appearance (entry into the blood) and glucose disposal (removal from the blood). In the healthy individual, the rates of appearance and disposal are essentially equal during exercise of moderate intensity and duration; however, prolonged exercise or sufficiently intense exercise can result in an imbalance leaning towards a higher rate of disposal than appearance, at which point glucose levels fall producing the onset of fatigue. Rate of glucose appearance is dictated by the amount of glucose being absorbed at the gut as well as liver (hepatic) glucose output. Although glucose absorption from the gut is not typically a source of glucose appearance during exercise, the liver is capable of catabolizing stored glycogen (glycogenolysis) as well as synthesizing new glucose from specific reduced carbon molecules (glycerol, pyruvate, and lactate) in a process called gluconeogenesis. The ability of the liver to release glucose into the blood from glycogenolysis is unique, since skeletal muscle, the other major glycogen reservoir, is incapable of doing so. Unlike skeletal muscle, liver cells contain the enzyme glycogen phosphatase, which removes a phosphate group from glucose-6-P to release free glucose. In order for glucose to exit a cell membrane, the removal of this phosphate group is essential. Although gluconeogenesis is an important component of hepatic glucose output, it alone can not sustain exercise. For this reason, when glycogen stores are depleted during exercise, glucose levels fall and fatigue sets in. Glucose disposal, the other side of the equation, is controlled by uptake of glucose at the working skeletal muscles. During exercise, despite decreased insulin concentrations, muscle increases GLUT4 translocation of and glucose uptake. The mechanism for increased GLUT4 translocation is an area of ongoing research.

glucose control: As mentioned above, insulin secretion is reduced during exercise, and does not play a major role in maintaining normal blood glucose concentration during exercise, but its counter-regulatory hormones appear in increasing concentrations. Principle among these are glucagon, epinephrine, and growth hormone. All of these hormones stimulate liver (hepatic) glucose output, among other functions. For instance, both epinephrine and growth hormone also stimulate adipocyte lipase, which increases non-esterified fatty acid (NEFA) release. By oxidizing fatty acids, this spares glucose utilization and helps to maintain blood sugar level during exercise.

Exercise for diabetes: Exercise is a particularly potent tool for glucose control in those who have diabetes mellitus. In a situation of elevated blood glucose (hyperglycemia), moderate exercise can induce greater glucose disposal than appearance, thereby decreasing total plasma glucose concentrations. As stated above, the mechanism for this glucose disposal is independent of insulin, which makes it particularly well-suited for people with diabetes. In addition, there appears to be an increase in sensitivity to insulin for approximately 1224 hours post-exercise. This is particularly useful for those who have type II diabetes and are producing sufficient insulin but demonstrate peripheral resistance to insulin signaling. However, during extreme hyperglycemic episodes, people with diabetes should avoid exercise due to potential complications associated with ketoacidosis. Exercise could exacerbate ketoacidosis by increasing ketone synthesis in response to increased circulating NEFA's.

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